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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, rats recovering from glycerol-induced acute renal failure were found to be protected from mercury-induced nephropathy, and HgCl2 poisoning protected rats from developing myohemoglobinuric renal failure. In view of the widely disparate nature of the renal failure models used, refractoriness appears to relate to an altered sensitivity of the organism itself rather than reflecting resistance to a particular nephropathic challenge. Renal renin content of the rats at the time of rechallenge was normal or high, a finding which contrasts sharply with that of chronically saline-loaded animals which also are refractory to ARF but have a maximally suppressed renal renin content. Renal renin depletion is not essential to the prevention of acute renal failure in the rat.
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PMID:Resistance to acute renal failure afforded by prior renal failure: examination of the role of renal renin content. 115 48

Erythrocyte structure was studied in rat after uranyl nitrate (UN:5 mg/kg) intoxication. The study of pathogenic progression of UN induced renal failure (ARF) was confined to the early initiation phase (2 hr), late initiation phase (8 hr) and the maintenance phase (24 hr). Erythrocyte structure has been found to be greatly influenced. The UN induced hemolytic syndrome/hypoxia was accompanied by a marked anisocytosis and poikilocytosis during different phases of ARF, which is characteristic of UN poisoning. Subsequent alterations in erythrocyte structure followed by UN administration or during the pathogenic progression of ARF has clinical and diagnostic importance as the alterations were much distinct prior to the clinical manifestation of ARF even at light microscopic level.
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PMID:Uranyl nitrate induced corpuscular derangement: an early indication of induced acute renal failure. 152 60

Eighty-two patients with acute pancreatis observed in the last seven years were included in prospective trial of monitoring protocol comprising: multiple organ failure and non invasive imaging of pancreatic lesion. One organ failure noted in the 60.9%, M.O.F. with three organ failure represented in the 21.9%. Renal failure was confirmed in 18.9%, trough nine clinical and biological index, become with shock in 73% and with extensive necrosis in 53%. ARF appeared with functional picture and normal diuresis in 73.3% and with organic failure in 26.7%. Index of specific mortality was 33.3%, while the comprehensive index of mortality in the study group was 12.9%, with a significant incidence in the half of deaths.
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PMID:[Kidney failure during acute pancreatitis. A unique aspect of multiple organ failure]. 210 Sep 74

We studied the clinical and pathological data for 334 patients age 65 or more who underwent renal biopsy for acute renal failure (ARF, n = 55), subacute renal failure (SRF, n = 72), chronic renal failure (CRF, n = 57), proteinuria (n = 137), and hematuria (n = 13). Tissue diagnoses were glomerulopathy (n = 252, 75.4%), acute tubular lesions (n = 18), interstitial nephritis (n = 23), vascular diseases (n = 36, including 14 with cholesterol emboli), and five miscellaneous diagnoses. Of the 55 patients with ARF, 23 had a glomerular lesion, 15 had acute tubular necrosis, and 8 had acute interstitial nephritis. Of 72 patients with SRF, 49 had a glomerulopathy, 12 had a vascular disorder, and six had acute interstitial nephritis. Hence, patients with ARF or SRF exhibited a high potential for reversible lesions. Only 11.3% of patients with CRF had potentially reversible causes. The most common causes of proteinuria were membranous glomerulopathy (34.3%), minimal change disease (14.6%), focal segmental sclerosis (11.7%), and amyloidosis (8.8%). Of the 25 patients with advanced nephrosclerosis, 24 had renal failure, 20 were hypertensive, and 13 had cholesterol emboli. Of 33 patients with diabetes mellitus, 66.7% were found to have lesions not related to diabetes. We conclude that renal biopsy is most useful in older patients with ARF or SRF because of potentially reversible renal disease. Old age alone is not a contraindication to performing a renal biopsy.
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PMID:Renal biopsy in patients 65 years of age or older. An analysis of the results of 334 biopsies. 235 29

The characteristics of exsorption and/or excretion of procainamide and its metabolite, N-acetylprocainamide (NAPA), into the small intestinal lumen in both normal rats and rats with acute renal failure (ARF rats) induced by uranyl nitrate were investigated by an in situ single-pass perfusion technique. The exsorption of procainamide and NAPA from blood into the intestinal lumen was increased in ARF rats compared with normal rats. The mean apparent renal, biliary and intestinal clearance values of procainamide were 186, 1.83 and 73.9 ml/h/kg in normal rats, respectively, and were 2.02, 1.37 and 55.8 ml/h/kg in ARF rats respectively. Furthermore, the mean renal, biliary and intestinal clearance values of NAPA were 35.2, 19.4 and 21.1 ml/h/kg in normal rats, respectively, and were 1.12, 21.0 and 26.0 ml/h/kg in ARF rats, respectively. There was little difference in the intestinal clearance values of procainamide and NAPA between normal and ARF rats. The ratio of nonrenal clearance/total body clearance was greater in ARF rats than in normal rats. Treatment with oral activated charcoal reduced the serum NAPA levels in both normal and ARF rats, and had little effect on the serum procainamide levels in normal rats, while it reduced the serum drug levels in ARF rats. Consequently, the increase in both drugs transported into the intestinal lumen induced by renal failure may enhance the intestinal clearance of the drug by oral administration of activated charcoal.
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PMID:Transport of procainamide and N-acetylprocainamide from blood into the intestinal lumen and intestinal dialysis by oral activated charcoal in rats with acute renal failure. 246 Jun 13

Animals with renal failure have a number of fairly predictable metabolic abnormalities. They are commonly presented to the veterinarian in a state of negative water balance, although prior fluid therapy in an oliguric patient may result in overhydration. Animals with oliguric ARF have sodium retention; those with polyuric ARF have increased urinary sodium loss. Chronic renal failure does not necessarily affect the ability of the renal tubule to conserve or excrete sodium, although the response to changes in sodium load is much slower than in the normal animal. Potassium retention occurs in oliguric ARF and potassium wasting in polyuric ARF; potassium balance is approximately normal in animals with CRF. Both ARF and CRF cause metabolic acidosis, although the acid-base status in a given animal will be affected by respiratory compensation, as well as other problems such as vomiting. Calcium levels are usually normal to slightly decreased in renal failure, whereas phosphorus levels are generally increased. The basic principles of fluid therapy should be used when constructing a plan for such therapy in an animal with renal failure. Intravenous administration of fluids is almost always necessary. The choice of the type of fluid, solutes, and electrolytes to be administered is based on the predicted abnormalities associated with renal failure as well as the laboratory abnormalities in the animal. Careful monitoring of the patient and periodic assessment of various laboratory parameters are necessary in order to make appropriate adjustments in fluid therapy.
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PMID:Fluid therapy for acute and chronic renal failure. 264 69

Acute renal failure has become a very rare complication of pregnancy. This results from the virtual disappearance of septic abortion ARF and from the improvement of prenatal care, including the prevention of volume contraction which is mainly due to uterine haemorrhage, early diagnosis, and treatment of other classic maternal complications such as pre-eclampsia and acute pyelonephritis. The incidence of BRCN has also been declining during the last decade. Acute fatty liver, a potentially fatal disease, is often complicated by ARF. Early recognition of this disorder with prompt termination of pregnancy and intensive supportive therapy can reduce fetal and maternal mortality rate. The syndrome of idiopathic postpartum renal failure is also associated with a high morbidity and mortality. Beyond supportive treatment including haemo- or peritoneal dialysis, the use of potent antihypertensive drugs to control blood pressure and blood transfusion if necessary, specific therapy as plasma infusion, plasma exchange and antiplatelet drugs may be of value. Both peritoneal dialysis and haemodialysis may be used in gravidas with ARF. Early 'prophylactic' dialysis should be applied to pregnant women. Careful monitoring of fluid balance and anticoagulation is necessary during dialysis.
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PMID:Acute renal failure in pregnancy. 333 Apr 90

High-dose intravenous urography (IVU) was performed 62 times in 59 patients with acute (ARF) and chronic (CRF) renal failure. The major diagnostic categories were chronic glomerulonephritis, malignant hypertension, acute tubular necrosis (ATN), and acute glomerulonephritis. The cause of the renal failure, whether CRF or ARF, oliguric or nonoliguric, could not be reliably determined by either the evolving pattern or density of nephrogram, or the size of the kidneys. Although a persistent dense nephrogram favored the diagnosis of ATN, the major correlate was a decreasing density of nephrogram as the serum creatinine level increased (P less than 0.005).
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PMID:Diagnostic role of intravenous urography in acute and chronic renal failure. 378 76

Kidney cortical and medullary "spin-lattice" (T1) and "spin-spin" (T2) relaxation times were measured by spectroscopy in several types of experimental renal failure in rats. The T1 and the measured tissue water content were used to calculate the fraction bound (FB) and hydration fraction (HF) according to a fast proton diffusion model. The present study demonstrated the possibility to differentiate between normal and pathological renal tissue resulting from renal artery clamping (RAC), renal pedicle clamping (RPC) with or without reflow, glycerol-induced acute renal failure with or without previous dehydration, and chronic hypertensive renal failure induced by 5/6 nephrectomy and saline loading, with low (6%) or normal (21%) protein diet. Shortened T1 and prolonged T2 found in both cortex and medulla of the glycerol-induced ARF in dehydrated rats seem to represent a MR ischemic pattern. The prolongation of T1 and T2 and the increase in water content in the other groups seem to relate to different amounts of tubular obstruction and renal congestion. In summary, characteristic MR properties of different types of renal failure may provide etiological and pathogenetic diagnostic possibilities.
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PMID:Proton magnetic resonance in experimental acute and chronic renal failure in rats. 382 4

The role of glucagon in the pathogenesis of abnormalities of glucose metabolism associated with renal failure remains undefined. We have evaluated glucagon-stimulated glucose and cyclic AMP output and amino acid uptake in isolated perfused livers of rats with experimentally-induced ARF and sham-operated controls. ARF animals exhibited azotemia, hyperglycemia, hyperinsulinemia, and hyperglucagonemia. During stimulation with physiologic (3 X 10-10M) or supraphysiologic (3 X 10-8M) glucagon concentrations, glucose output was lower in livers of ARF rats than in those of controls, whereas cyclic AMP responses were similar or exceeded those of controls. Hepatic glycogen content was lower in rats with ARF and the stores were exhausted at the end of perfusions. Additional studies in livers of fasted animals revealed no significant differences in glucose output or amino acid uptake between ARF and control livers perfused with physiologic levels of glucagon. These experiments suggest that the decreased glucagon-stimulated glucose output in isolated perfused livers in acutely uremic rats is due primarily to glycogen depletion rather than to impaired gluconeogenesis. Normal or increased cyclic AMP responses to glucagon suggests intactness of the hormone receptor-adenylate cyclase.
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PMID:Impaired glucagon-stimulated glucose output in livers of acutely uremic rats. 627 48


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